Affiliation:
1. From the Institute of Urology and Nephrology (W.R.J.W., C.H.F.), University College London, and Academic Cardiology Unit (M.C., D.J.S.), St. Mary’s Hospital Medical School, London, UK.
Abstract
Abstract
The impedance to current flow in the intracellular compartment of guinea pig left ventricular myocardium was measured at 20°C and 37°C using tissue from hypertrophied hearts subjected to aortic constriction. Alternating current of varying frequency was passed longitudinally along myocardial preparations, which revealed two time constants: one attributed to the surface membrane at the ends of the preparation and a second lying in the intracellular pathway. The longitudinal impedance was quantitatively analyzed in terms of a parallel intracellular and extracellular pathway; the former had two series components, one attributable to the sarcoplasm and the other to the low-resistance junctions between adjacent cells. This interpretation was consistent (1) with control experiments using
n
-heptanol, which increased the component attributed to intercellular junctions but not sarcoplasmic resistivity, and (2) with suspensions of isolated myocytes, which yielded a similar value for the sarcoplasmic resistivity. Aortic constriction increased the heart weight–to–body weight ratio of experimental animals from a mean value of 3.10±0.28 to 5.05±0.83 g/kg after 50 days of constriction and 5.60±0.95 g/kg after 150 days of constriction. An increase of heart weight–to–body weight ratio at 150 days of constriction was associated with an increased intracellular resistivity, which could be attributed solely to an increase of the junctional resistance between adjacent cells by ≈44% at 20°C and 140% at 37°C; the sarcoplasmic resistivity was unchanged. The results are discussed in terms of altered conduction in hypertrophied myocardium as a possible basis for arrhythmias in this tissue.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine,Physiology
Reference32 articles.
1. Risk of ventricular arrhythmias in left ventricular hypertrophy: The Framingham Heart Study
2. Mechanisms of ventricular arrhythmias in cardiac failure and hypertrophy
3. Aguilar JC Martinez AH Conejos FA. Mechanisms of ventricular arrhythmias in the presence of pathological hypertrophy. Eur Heart J . 1993;14(suppl J):65-70.
4. Aronson RS Ming Z. Cellular mechanisms of arrhythmias in hypertrophied and failing myocardium. Circulation . 1993;87(suppl VII):VII-76-VII-83.
Cited by
72 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献